Metabolic vulnerability identified in small cell lung cancer
Researchers at the University of Cologne have demonstrated that, while various cellular states of small cell lung cancer are equally dependent on the amino acid cysteine, they react differently when deprived of it. While some cancer cells subsequently die via ferroptosis—a form of cell death in which harmful oxidized fats accumulate in the cell membranes—others undergo apoptosis, a controlled,…
Researchers at the University of Cologne have discovered that small cell lung cancer cells rely on the amino acid cysteine, regardless of their cellular state. However, when cysteine is taken away, these cells react differently. Some die through ferroptosis, a process where harmful oxidized fats accumulate in cell membranes, while others undergo apoptosis, a controlled cell death.
A new study reveals that a protein called ASCL1, which regulates cell states, determines which response occurs. Cells with low ASCL1 levels die from ferroptosis, while those with high ASCL1 levels resist this cell death by activating a gene that produces antioxidants. Blocking this antioxidant defense in combination with cysteine deprivation slowed tumor growth in preclinical models.
These findings suggest that targeting cysteine dependence and ASCL1-mediated defenses could be a new therapeutic approach for treating small cell lung cancer.
Written by urgent.news from Medical Xpress's reporting — not their text. Machine-written — may contain errors; check the original before relying on it.
